2025年6月10日 周二
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Progress on the role of inflammatory cells in atherosclerosis
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Affiliation:

1.Shanxi Medical University, Taiyuan, Shanxi 030001, China;2.Department of Cardiovascular Medicine, the Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China)

Clc Number:

R5

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    Abstract:

    Cardiovascular disease (CVD) is a serious threat to human health. Atherosclerosis (As), as an important pathological basis of CVD, is a chronic immune inflammatory disease caused by the deposition of oxidized lipid in the vascular wall. Various immune inflammatory cells play a key role in the occurrence and development of As, so it is very important to explore the mechanism of immune cells in the pathological changes to study the treatment strategy of CVD.In this paper, the functions of neutrophils, monocytes, lymphocytes, dendritic cells and mast cells in As are reviewed.

    Reference
    [1] GROOT H E, VAN BLOKLAND I V, LIPSIC E, et al.Leukocyte profiles across the cardiovascular disease continuum:a population-based cohort study.J Mol Cell Cardiol, 0,8:158-164.
    [2] DRECHSLER M, MEGENS R T, VAN ZANDVOORT M, et al.Hyperlipidemia-triggered neutrophilia promotes early atherosclerosis.Circulation, 0,2(18):1837-1845.
    [3] 胡国晶, 路娇扬, 王双.Toll样受体与动脉粥样硬化易损斑块的关系.中国动脉硬化杂志, 2,0(5):477-480.
    [4] 左海奇, 李碧澄, 田野.中性粒细胞胞外陷阱网在动脉粥样硬化进展中的作用.中国动脉硬化杂志, 7,5(6):635-639.
    [5] SAHINARSLAN A, KOCAMAN S A, BAS D, et al.Plasma neutrophil gelatinase-associated lipocalin levels in acute myocardial infarction and stable coronary artery disease.Coron Artery Dis, 1,2(5):333-338.
    [6] SMITH C K, VIVEKANANDAN-GIRI A, TANG C, et al.Neutrophil extracellular trap-derived enzymes oxidize high-density lipoprotein:an additional proatherogenic mechanism in systemic lupus erythematosus.Arthritis Rheumatol, 4,6(9):2532-2544.
    [7] SILVESTRE-ROIG C, BRASTER Q, WICHAPONG K, et al.Externalized histone H4 or chestrates chronic inflammation by inducing lytic cell death.Nature, 9,9(7755):236-240.
    [8] MANGOLD A, ALIAS S, SCHERZ T, et al.Coronary neutrophil extracellular trap burden and deoxyribonuclease activity in ST-elevation acute coronary syndrome are predictors of ST-segment resolution and infarct size.Circ Res, 5,6(7):1182-1192.
    [9] ELASKALANI O, ABDOL R N, METHAROM P.Neutrophil extracellular traps induce aggregation of washed human platelets independently of extracellular DNA and histones.Cell Commun Signal, 8,6(1):24.
    [10] REYES-GARCA A, AROCA A, ARROYO A B, et al.Neutrophil extracellular trap components increase the expression of coagulation factors.Biomed Rep, 9,0(3):195-201.
    [11] GOULD T J, VU T T, SWYSTUN L L, et al.Neutrophil extracellular traps promote thrombin generation through platelet-dependent and platelet-independent mechanisms.Arterioscler Thromb Vasc Biol, 4,4(9):1977-1984.
    [12] SEIF K, ALIDZANOVIC L, TISCHLER B, et al.Neutrophil-mediated proteolysis of thrombospondin-1 promotes platelet adhesion and string formation.Thromb Haemost, 8,8(12):2074-2085.
    [13] GOMEZ I, WARD B, SOUILHOL C, et al.Neutrophil microvesicles drive atherosclerosis by delivering miR-155 to atheroprone endothelium.Nat Commun, 0,1(1):214.
    [14] JAIPERSAD A S, SHANTSILA A, LIP G Y, et al.Expression of monocyte subsets and angiogenic markers in relation to carotid plaque neovascularization in patients with pre-existing coronary artery disease and carotid stenosis.Ann Med, 4,6(7):530-538.
    [15] AMMIRATI E, MORONI F, MAGNONI M, et al.Circulating CD14+ and CD14(high)CD16- classical monocytes are reduced in patients with signs of plaque neovascularization in the carotid artery.Atherosclerosis, 6,5:171-178.
    [16] MEEUWSEN J, DE VRIES J J, VAN DUIJVENVOORDE A, et al.Circulating CD14(+)CD16(-) classical monocytes do not associate with a vulnerable plaque phenotype, and do not predict secondary events in severe atherosclerotic patients.J Mol Cell Cardiol, 9,7:260-269.
    [17] YAMAMOTO H, YOSHIDA N, SHINKE T, et al.Impact of CD14(++)CD16(+) monocytes on coronary plaque vulnerability assessed by optical coherence tomography in coronary artery disease patients.Atherosclerosis, 8,9:245-251.
    [18] SAHBANDAR I N, NDHLOVU L C, SAIKI K, et al.Relationship between Circulating Inflammatory Monocytes and Cardiovascular Disease Measures of Carotid Intimal Thickness.J Atheroscler Thromb, 0,7(5):441-448.
    [19] LO S C, LEE W J, CHEN C Y, et al.Intermediate CD14(++)CD16(+) monocyte predicts severe coronary stenosis and extensive plaque involvement in asymptomatic individuals.Int J Cardiovasc Imaging, 7,3(8):1223-1236.
    [20] MARCOVECCHIO P M, THOMAS G D, MIKULSKI Z, et al.Scavenger receptor CD36 directs nonclassical monocyte patrolling along the endothelium during early atherogenesis.Arterioscler Thromb Vasc Biol, 7,7(11):2043-2052.
    [21] ONG S M, HADADI E, DANG T M, et al.The pro-inflammatory phenotype of the human non-classical monocyte subset is attributed to senescence.Cell Death Dis, 8,9(3):266.
    [22] URBANSKI K, LUDEW D, FILIP G, et al.CD14(+)CD16(++) “nonclassical” monocytes are associated with endothelial dysfunction in patients with coronary artery disease.Thromb Haemost, 7,7(5):971-980.
    [23] VU D M, TAI A, TATRO J B, et al.γδT cells are prevalent in the proximal aorta and drive nascent atherosclerotic lesion progression and neutrophilia in hypercholesterolemic mice.PLoS One, 4,9(10):e109416.
    [24] KANG K, BACHU M, PARK S H, et al.IFN-γ selectively suppresses a subset of TLR4-activated genes and enhancers to potentiate macrophage activation.Nat Commun, 9,0(1):3320.
    [25] 谈春芝, 谭玉林, 姚峰, 等.白细胞介素4对THP-1巨噬细胞三磷酸腺苷结合盒转运体A1表达和胆固醇流出的影响.中国动脉硬化杂志, 5,3(12):1203-1209.
    [26] BINDER C J, HARTVIGSEN K, CHANG M K, et al.IL-5 links adaptive and natural immunity specific for epitopes of oxidized LDL and protects from atherosclerosis.J Clin Invest, 4,4(3):427-437.
    [27] SRIKAKULAPU P, UPADHYE A, ROSENFELD S M, et al.Perivascular adipose tissue harbors atheroprotective IgM-producing B cells.Front Physiol, 7,8:719.
    [28] CARDILO-REIS L, GRUBER S, SCHREIER S M, et al.Interleukin-13 protects from atherosclerosis and modulates plaque composition by skewing the macrophage phenotype.EMBO Mol Med, 2,4(10):1072-1086.
    [29] SHIOTSUGU S, OKINAGA T, HABU M, et al.The biological effects of interleukin-17A on adhesion molecules expression and foam cell formation in atherosclerotic lesions.J Interferon Cytokine Res, 9,9(11):694-702.
    [30] OWCZARCZYK-SACZONEK A, PLACEK W.Interleukin-17 as a factor linking the pathogenesis of psoriasis with metabolic disorders.Int J Dermatol, 7,6(3):260-268.
    [31] JEON U S, CHOI J P, KIM Y S, et al.The enhanced expression of IL-17-secreting T cells during the early progression of atherosclerosis in ApoE-deficient mice fed on a western-type diet.Exp Mol Med, 5,7(5):e163.
    [32] LIN Y Z, WU B W, LU Z D, et al.Circulating Th22 and Th9 levels in patients with acute coronary syndrome.Mediators Inflamm, 3,3:635672.
    [33] SHI L, JI Q, LIU L, et al.IL-22 produced by Th22 cells aggravates atherosclerosis development in ApoE－/－ mice by enhancing DC-induced Th17 cell proliferation.J Cell Mol Med, 0,4(5):3064-3078.
    [34] FOKS A C, FRODERMANN V, ter BORG M, et al.Differential effects of regulatory T cells on the initiation and regression of atherosclerosis.Atherosclerosis, 1,8(1):53-60.
    [35] THOTA L N, PONNUSAMY T, PHILIP S, et al.Author correction:immune regulation by oral tolerance induces alternate activation of macrophages and reduces markers of plaque destabilization in ApoB(tm2Sgy)/Ldlr(tm1Her/J) mice.Sci Rep, 8,8(1):15974.
    [36] SHARMA M, SCHLEGEL M P, AFONSO M S, et al.Regulatory T cells license macrophage pro-resolving functions during atherosclerosis regression.Circ Res, 0,7(3):335-353.
    [37] BURGER F, MITEVA K, BAPTISTA D, et al.Follicular regulatory helper T cells control the response of regulatory B cells to a high-cholesterol diet.Cardiovasc Res, 1,7(3):743-755.
    [38] COCHAIN C, KOCH M, CHAUDHARI S M, et al.CD8+ T cells regulate monopoiesis and circulating Ly6C-high monocyte levels in atherosclerosis in mice.Circ Res, 5,7(3):244-253.
    [39] VAN DUIJN J, KRITIKOU E, BENNE N, et al.CD8+ T-cells contribute to lesion stabilization in advanced atherosclerosis by limiting macrophage content and CD4+ T-cell responses.Cardiovasc Res, 9,5(4):729-738.
    [40] HOSSEINI H, LI Y, KANELLAKIS P, et al.Phosphatidylserine liposomes mimic apoptotic cells to attenuate atherosclerosis by expanding polyreactive IgM producing B1a lymphocytes.Cardiovasc Res, 5,6(3):443-452.
    [41] KYAW T, TIPPING P, BOBIK A, et al.Opposing roles of B lymphocyte subsets in atherosclerosis.Autoimmunity, 7,0(1):52-56.
    [42] ROSENFELD S M, PERRY H M, GONEN A, et al.B-1b cells secrete atheroprotective IgM and attenuate atherosclerosis.Circ Res, 5,7(3):e28-e39.
    [43] RINCN-ARVALO H, VILLA-PULGARN J, TABARES J, et al.Interleukin-10 production and T cell-suppressive capacity in B cell subsets from atherosclerotic ApoE－/－ mice.Immunol Res, 7,5(5):995-1008.
    [44] NUS M, SAGE A P, LU Y, et al.Marginal zone B cells control the response of follicular helper T cells to a high-cholesterol diet.Nat Med, 7,3(5):601-610.
    [45] DOUNA H, AMERSFOORT J, SCHAFTENAAR F H, et al.Bidirectional effects of IL-10(+) regulatory B cells in LDLR－/－ mice.Atherosclerosis, 9,0:118-125.
    [46] CHOI J H, CHEONG C, DANDAMUDI D B, et al.Flt3 signaling-dependent dendritic cells protect against atherosclerosis.Immunity, 1,5(5):819-831.
    [47] HADDAD Y, LAHOUTE C, CLMENT M, et al.The dendritic cell receptor DNGR-1 promotes the development of atherosclerosis in mice.Circ Res, 7,1(3):234-243.
    [48] CLEMENT M, RAFFORT J, LAREYRE F, et al.Impaired autophagy in CD11b(+) dendritic cells expands CD4(+) regulatory T cells and limits atherosclerosis in mice.Circ Res, 9,5(11):1019-1034.
    [49] WEBER C, MEILER S, DRING Y, et al.CCL17-expressing dendritic cells drive atherosclerosis by restraining regulatory T cell homeostasis in mice.J Clin Invest, 1,1(7):2898-2910.
    [50] YE Y, YANG X, ZHAO X, et al.Serum chemokine CCL17/thymus activation and regulated chemokine is correlated with coronary artery diseases.Atherosclerosis, 5,8(2):365-369.
    [51] SAGE A P, MURPHY D, MAFFIA P, et al.MHC class II-restricted antigen presentation by plasmacytoid dendritic cells drives proatherogenic T cell immunity.Circulation, 4,0(16):1363-1373.
    [52] YUN T J, LEE J S, MACHMACH K, et al.Indoleamine 2,3-dioxygenase-expressing aortic plasmacytoid dendritic cells protect against atherosclerosis by induction of regulatory T cells.Cell Metab, 6,3(5):852-866.
    [53] DAISSORMONT I T, CHRIST A, TEMMERMAN L, et al.Plasmacytoid dendritic cells protect against atherosclerosis by tuning T-cell proliferation and activity.Circ Res, 1,9(12):1387-1395.
    [54] KRITIKOU E, DEPUYDT M, de VRIES M R, et al.Flow cytometry-based characterization of mast cells in human atherosclerosis.Cells, 9,8(4):334.
    [55] KRITIKOU E, VAN DUIJN J, NAHON J E, et al.Disruption of a CD1d-mediated interaction between mast cells and NKT cells aggravates atherosclerosis.Atherosclerosis, 9,0:132-139.
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WANG Min, LI Jin. Progress on the role of inflammatory cells in atherosclerosis[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2022,30(3):265-270.

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History
  • Received:August 07,2020
  • Revised:June 07,2021
  • Online: January 14,2022
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